Transposons have been shown to play major roles in spontaneous mutation in Drosophila and other eukaryotes. In chromosomes, the insertion or excision of these mobile elements disrupts gene function at the site of insertion or may create deletions if excision is not precise. Additionally, recombination between two copies of a transposon situated at different sites in a chromosome or in homologs produces a variety of chromosomal rearrangements, depending on the orientation of the paired mobile elements. We are studying rearrangements produced by these types of ectopic recombination to determine the molecular structures at their breakpoint junctions and to learn more about how transposons mediate these types of asymmetrical exchanges. We have found that interchromosomal and intrachromosomal ectopic recombination are equally frequent. Homozygosis for transposon insertions and other sequence variations greatly diminishes ectopic recombination.